Albert Stewart G, Mooradian Arshag D
Division of Endocrinology, Diabetes, and Metabolism, Department of Internal Medicine, St. Louis University School of Medicine, St. Louis, Missouri 63104, USA.
J Clin Endocrinol Metab. 2004 Feb;89(2):695-701. doi: 10.1210/jc.2003-031264.
Obese individuals are in a reduced GH/IGF-I state that may be maladaptive. Fifty-nine obese men and premenopausal menstruating women (body mass index, 36.9 +/- 5.0 kg/m(2)) were randomized to a double-blind, placebo-controlled trial of low dose recombinant human GH (rhGH). During the 6-month intervention, subjects self-administered daily rhGH or equivalent volume of placebo at 200 micro g (1.9 +/- 0.3 microg/kg for men, 2.0 +/- 0.3 microg/kg for women); after 1 month, the dose was increased to 400 microg (3.8 +/- 0.5 microg/kg) in men and 600 microg (6.0 +/- 0.8 microg/kg) in women. rhGH was then discontinued, and subjects were followed up after 3 months. Forty completed the intervention, and 39 completed the follow-up. Drop-out rates between rhGH vs. placebo groups were not different (chi(2) = 1.45; P = 0.228). One subject discontinued the drug due to an rhGH-related side effect. Body weight (BW) decreased with rhGH from 100.4 +/- 13.2 to 98.0 +/- 15.6 kg at 6 months (P = 0.04) and was sustained at 98.1 +/- 16.6 kg at 9 months (P = 0.02). BW loss was entirely due to loss of body fat (BF). Intention to treat analyses demonstrated changes from baseline between rhGH and placebo in BW (-2.16 +/- 4.48 vs. -0.04 +/- 2.67 kg; P = 0.03) and BF (-2.89 +/- 3.76 vs. -0.68 +/- 2.37 kg; P = 0.01). rhGH increased IGF-I from -0.72 to +0.10 SD (P = 0.0001). rhGH increased high-density lipoprotein cholesterol 19% from 1.11 +/- 0.34 to 1.32 +/- 0.28 mmol/liter (P < 0.001). Neither group had changes in fasting glucose, insulin sensitivity, or resting energy expenditure. In conclusion, in obesity, rhGH normalized IGF-I levels, induced loss of BW from BF, and improved lipid profile without untoward effects on insulin sensitivity.
肥胖个体处于生长激素/胰岛素样生长因子-1（GH/IGF-I）水平降低的状态，这可能是适应不良的。59名肥胖男性和绝经前有月经的女性（体重指数，36.9±5.0kg/m²）被随机分配到一项低剂量重组人生长激素（rhGH）的双盲、安慰剂对照试验中。在为期6个月的干预期间，受试者每天自行注射rhGH或等量的安慰剂，剂量为200μg（男性为1.9±0.3μg/kg，女性为2.0±0.3μg/kg）；1个月后，男性剂量增加到400μg（3.8±0.5μg/kg），女性增加到600μg（6.0±0.8μg/kg）。然后停止使用rhGH，并在3个月后对受试者进行随访。40名受试者完成了干预，39名完成了随访。rhGH组与安慰剂组的退出率没有差异（χ²=1.45；P=0.228）。一名受试者因rhGH相关的副作用而停药。6个月时，rhGH组体重（BW）从100.4±13.2kg降至98.0±15.6kg（P=0.04），9个月时维持在98.1±16.6kg（P=0.02）。体重减轻完全是由于体脂（BF）减少。意向性分析显示，rhGH组与安慰剂组相比，BW从基线的变化为（-2.16±4.48 vs.-0.04±2.67kg；P=0.03），BF为（-2.89±3.76 vs.-0.68±2.37kg；P=0.01）。rhGH使IGF-I从-0.72标准差增加到+0.10标准差（P=0.0001）。rhGH使高密度脂蛋白胆固醇从1.11±0.34mmol/L增加19%至1.32±0.28mmol/L（P<0.001）。两组的空腹血糖、胰岛素敏感性或静息能量消耗均无变化。总之，在肥胖患者中，rhGH使IGF-I水平正常化，导致体脂引起的体重减轻，并改善了血脂谱，而对胰岛素敏感性没有不良影响。
